Benefits of a Standardized Enteral Feeding Protocol on the Nutrition and Health Outcomes of Very Low Birth Weight Preterm Infants.

To compare nutrition and health outcomes before and after implementing a standardized enteral feeding protocol on nutrition and health outcomes in very low birth weight preterm infants. A retrospective chart review was performed evaluating preterm infants, born less than 34 weeks gestation and weighing less than 1500 g, before and after the implementation of a standardized enteral feeding protocol. Outcomes included weaning of parenteral nutrition, initiation and advancement of enteral feeds, initiation of human-milk fortifier (HMF), change in weight -score and neonatal morbidities.

Evaluation of Methods of Breast or Bottle Feeding on Length of Hospitalization of Preterm Infants.

Direct breastfeeding is the optimal method of nourishing preterm infants. Preconceived notions exist among health practitioners that establishment of direct breastfeeding lengthens hospitalization. Thus far, the aforementioned association remains unknown.

Determinants of Successful Direct Breastfeeding at Hospital Discharge in High-Risk Premature Infants.

Background: Despite a mother's intention to breastfeed, there are many barriers to feeding preterm infants that decrease breastfeeding rates.

Objective: The objective of this research was to determine factors associated with successful direct breastfeeding (DBF) of the preterm infant at hospital discharge.

Materials And Methods: A retrospective chart review of 69 preterm (<34 weeks' gestational age) infants in the neonatal intensive care unit, whose mothers intended to breastfeed, was conducted.

Does the use of oral nonabsorbable antifungal prophylaxis reduce the incidence of fungal colonization and/or systemic infection in preterm infants?

Background: Invasive fungal infection is a significant cause of mortality and morbidity in preterm infants. Oral nonabsorbable agents are used prophylactically, but the literature regarding their effectiveness has not been systematically reviewed.

Objective: To determine if oral nonabsorbable antifungal prophylaxis reduces the incidence of fungal colonization and/or systemic infection in preterm infants.

Hyperthermia amplifies brain cytokine and reactive oxygen species response in a model of perinatal inflammation.

Chorioamnionitis, a perinatal infection of the fetal membranes, and maternal fever, which often accompanies infection are both risk factors for cerebral palsy (CP). Inflammation is a typical reaction to infection. Thus the aim of this study was to determine if hyperthermia alters newborn rat brain inflammatory response and oxidant stress after a maternal rat lipopolysaccaharide (LPS) injection.

Corticotropin-releasing hormone potentiates neural injury induced by oxygen-glucose deprivation: a possible involvement of microglia.

While corticotropin-releasing hormone (CRH) has been implicated in a variety of brain disorders such as ischemic injury, the molecular mechanism by which CRH elicits its activities is largely unclear. In the present study, we have determined the effect of CRH on oxygen-glucose deprivation (OGD) induced apoptosis in fetal hippocampal neurons. CRH alone at concentrations of 10-200 nM had no effect on neuronal apoptosis.

Systemic adrenocorticotropic hormone administration down-regulates the expression of corticotropin-releasing hormone (CRH) and CRH-binding protein in infant rat hippocampus.

Systemic adrenocorticotropic hormone (ACTH) administration is a first-line therapy for the treatment of infantile spasms, an age-specific seizure disorder of infancy. It is proposed that exogenous ACTH acts via negative feedback to suppress the synthesis of corticotropin-releasing hormone (CRH), a possible endogenous convulsant in infant brain tissue. The aim of this study was to determine whether systemic ACTH treatment in infant rats down-regulates the hippocampal CRH system, including CRH, CRH-binding protein (CRH-BP), and CRH receptors (CRH-R1 and CRH-R2).

Corticotropin-releasing hormone induces proliferation and TNF-alpha release in cultured rat microglia via MAP kinase signalling pathways.

We have previously demonstrated that corticotropin-releasing hormone (CRH) receptor 1 (CRH-R1) is functionally expressed in rat microglia. In the present study, we show that CRH, acting on CRH-R1, promoted cell proliferation and tumour necrosis factor-alpha (TNF-alpha) release in cultured rat microglia. Exogenous CRH resulted in an increase in BrdU incorporation compared with control cells, which was observed in a range of concentrations of CRH between 10 and 500 nm, with a maximal response at 50 nm.

Functional expression of corticotropin-releasing hormone (CRH) receptor 1 in cultured rat microglia.

Corticotropin-releasing hormone (CRH), known as a key regulator of the hypothalamic-pituitary-adrenal axis response to stress, elicits its biological effects by binding to two membrane receptors (CRH-R1 and CRH-R2). The present studies examined the presence of functional expression of CRH receptors in cultured microglia of rat. CRH-R1 mRNA and protein were detected by reverse transcriptase polymerase chain reaction (RT-PCR), western blotting and receptor chemical cross-linking assay in cultured microglia.